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Monday, December 26, 2011

I recently heard
a radio interview with Dr I. Eatwell (I can’t remember her real name but she
was a Californian food-head) who told us about her weekly cycle jaunt out of
the small town of Davis in California to pick wild herbs.We were, of course, all supposed to
gasp in admiration at her zeal to seek and eat local. In a sense, she was
emulating the famous French aristocrat who suggested that, in view of the
shortage of bread: "Qu'ils mangent de la brioche" or “Let them eat
cake”. Quite simply, there are not sufficient wild herbs to meet the
gastronomic needs of the firm and courageous citizens of even a small town such
as Davis. Moreover, since Dr I. Eatwell harvested the herbs before the seeding
period, she selfishly pulled the plug on food chain sustainability. The concept
of local food is elitist and unworkable for the general population. So let’s do
the sums. According to Sustainable Table, we should confine our food choice to
100 km radius. Lets extend that to 120 km to allow for the area of a large city.
That translates into about 4524 hectares which if farmed for wheat would yield
38,798,324 kg of wheat, translating into 27,158,826 kg of flour or
108,635,307,000 calories. Assuming a daily energy need of just 2,000 calories,
we would have enough to feed about 150 persons a year.So the theory works for towns with a
population up to 150,000 and of course the nearest other town must be 240 km
away, otherwise there would be territorial battles where their circles overlap.
It just doesn’t work for today’s demography. Of course a few privileged elite
can easily achieve this but its cake for the rest of us.

One of the smart
things mad did which no other species achieved was the division of labour:
“I’ll buy the peas you grow on your farm and you can buy tractor insurance from
me”.The chore of being
responsible for the provision of our own food was passed on to farmers who in
turn passed on responsibility for education, power and so forth. Many centuries
ago, those farmers were local but as modern transport evolved, we bought food
that was grown far away, often continents away. And so the high priests of
healthy eating introduced the concept of “food miles” and “eating in season”. I
will surely eat a strawberry this Christmas or find one on my champagne glass
and I’m not in the least bit bothered that it might come from Spain or Greece.
And I might concede that if I were to pluck a fresh strawberry in season in
County Wexford it would taste better than the imported and out-of-season
variety. But that imported and out-of-season variety still is unmistakably
strawberry in every olfactory sense if you’ll excuse the pun (did I just
punnet!). Not only does it taste and smell of strawberry, but it has the exact
nutritional composition that the in-season County Wexford strawberry has and I
can vary my diet to include imported and out-of-season fish, fruit, vegetables,
yams and so on. The overall health of the nation would improve if we were to
eat more fruit and more vegetables. Any implication that these foods have to be
sourced locally and in-season is utterly unhelpful.

Food miles are
another obsession with the high priests of health eating. The implication of
counting food miles is that local is best and the greater the food mile the
greater the sin. As ever, when put under the microscope, things are not so
straightforward. An apple, grown locally and sold at the end of the season just
before a new harvest, carries little mileage but it has consumed a significant
quantity of energy keeping it nice and juicy through autumn and into spring.
Without that energy consuming technological intervention, the apples would
rot.In contrast, a New
Zealand apple, just harvested in that beautiful country and consumed in Dublin
carries huge mileage but has used relatively little energy. Locally grown low
mileage tomatoes require a glasshouse and yet more energy while imported ones
are grown where the sun shines all day, yielding high mileage and low energy. And of course, one of the biggest
contributors to the energy cost of food occurs when it leaves the supermarket
shelf. Driving there and back, freezing, chilling and cooking food all gobbles
up energy. And of course, there is food waste. Sin scéal eile, which, for the Sassenachs
among you, translates into: “That’s another story”

Monday, December 19, 2011

According to the
experts and politicos in public health nutrition, the greatest food-related
condition on the planet is obesity.That is not so. The fat and overweight all over the world will enjoy
hearty feasts this Christmas or at their equivalent major holiday. It is hunger that is the greatest food-related
condition facing mankind. One billion of the globe’s citizens will go to bed
hungry on Christmas night, as they do every night. That is one in 6 of our
fellow humans.They live mostly in
South Asia and in sub-Saharan Africa. By 2050, over 95% of the growth in the
global population to 9 billion will be in these two regions. So too will be the
worst effects of climate change in reducing agricultural output. Aside from the
de-humanizing effect of hunger, there follows in its food steps a whole slew of
diseases, mostly infectious diseases, caused by a greatly impaired immune
system.The consequent daily death
rate from hunger is equivalent to 30 fully laden jumbo jets crashing each and
every day with all lives on board lost. Never forget that statistic.

The hungry are
not forgotten of course. They are constantly in our thoughts and most
importantly in the thoughts of our political leaders and our major global
agencies. They have been in their thoughts for the last 50 years as the
following quotes show:

We have the ability, we have the means, and
we have the capacity to eliminate hunger from the face of the earth. We need
only the will.

President John
F. Kennedy, 1963

Within one decade no child will go to bed
hungry, no family will fear for its next day’s bread, and no human being’s
future and capacities will be stunted by malnutrition. Every man, woman and
child has the inalienable right to be free from malnutrition and hunger

World Food
Conference, Rome, 1974

As a basis for the Plan of Action for
Nutrition . . . we pledge to make all efforts to eliminate before the end of
this decade: famine and famine-related deaths; starvation and nutritional
deficiency diseases in communities affected by natural and man-made disasters;
iodine and vitamin A deficiencies.

World
Declaration and Plan of Action for Nutrition, Rome, December 1992

The Rome Declaration calls upon us to reduce
by half the number of chronically undernourished people on the Earth by the
year 2015 . . . If each of us gives his or her best I believe that we can meet
and even exceed the target we have set for ourselves.

World Food
Summit 1996

Goal 1: Eradicate extreme poverty and
hunger; Target 2. Halve, between 1990 and 2015, the proportion of people who
suffer from hunger.

UN Millennium Development Goals 2002

We have seen in
the present crisis among the states of the euro zone a generally selfish
attitude of individual member states. On a global basis, a similarly selfish
attitude has impeded progress with regard to climate change. In each case, the
individual member states have a strategic interest, which is influenced by its
business community and by many non-governmental organisations.What hope has hunger got? The various
quotations above show that we are kidding ourselves and paying lip service to
the problem. In his book ‘Common wealth:
Economics of a crowded planet’ the distinguished leader in development
studies Jeffrey Sachs points out the need for a global solution to the problem.
But how can we persuade the business and NGO communities in Ireland and
elsewhere that global hunger is an issue of major importance and of sufficient
importance to merit significantly more investment than we give at present? “We
are in a recession” might be the general response. For the hungry, there is no
recession since you can only recess from what has been progressed and, in their
case, there has been no progression. Africa can help itself but not without our
help. So, right now, take out the credit card and in multiples of 6 make a
donation now to your favourite aid agency. If you don’t know of one
immediately, try my favourite: https://www.concern.net/donate.

Monday, December 12, 2011

Measuring our
dietary patterns and linking it to patterns of disease is at the core of modern
nutritional epidemiology and such data drive national and global food and
nutrition policy. There is, however, a serious and inherent flaw in the
measurement of food intake which modern nutritional epidemiology tends to
forget. That flaw is energy under-reporting. Our energy requirements are
composed of several factors, the most important of which is resting metabolism
which accounts for about 85% of energy needs in a normal adult following a
typical sedentary western lifestyle. These energy needs are to keep our hearts
beating, our lungs breathing, our kidneys filtering, our brains remembering and
so on. We can directly measure this as a person’s resting metabolic rate (RMR)
using a calorimeter and there are also a number of ways of doing so indirectly,
some of which areextremely
accurate. We can also calculate our RMR using a number of equations and you’ll
find plenty of calculators on the internet. My RMR is 2,030 calories. Because
I’m sedentary, except for golf on a Saturday morning, I need to up that figure
by about 15% to 2,335 calories to take account of my daily ohysical activity. A
very sporty person would have a higher multiplier of RMR.If I was a volunteer in a dietary
survey and I reported an energy intake of 1,900 calories, then ocviously I must
be dieting. If I say I’m not dieting and that this is a typical dietary intake,
then I’m under-reporting. There never has been and there probably never will be
a large survey, large enough to be of value to epidemiology, which does not
have some element of under-reporting. And the level of under-reporting is huge
- anywhere from 30% to 50%. We know this to be so using both simple equations
to measure RMR and also using very sophisticated stable isotopes.

Why do people
under-report? We know it is higher among females amd we know it increases with
increasing body weight. My explanation, which is not based on any experimental
data but on supposition is as follows. Most people with a western sedentary
lifestyle, have at some time sought to lose weight. They inevitably start on
Monday morning. Come Thursday, something happens, good or bad and the dieting
pattern is gone. Its back to normal to start all over again next Monday
morning. This cyclical pattern is familiar to many people. So, when asked to
take part in a dietary survey and when pressed to be truthful in every way to
report their habitual intake, which days do they deem to be “typical?. I’m
afraid that 30-50% of people deem the dietary restrictive days of Monday,
Tuesday and Wednesday to be normal. Thus they don’t deliberately lie but they
do under-report their food intake. In effect, food intake data are flawed and we
have to live with that for now until we come up with some smart way of
overcoming this problem.

Because
under-reporting is higher among the over-weight and obese, many assume that the
foods that are under-reported tend to be the so called “guilty” ones: foods
high in sugar and fats such as fast food, soft drinks, savoury snacks and so
on. This assumption is of course false since obesity is associated with ALL
foods (see blog of November 6th: “Taxing the fat and sweet”). Not surprisingly,
when we examine food intake data in those with plausible energy intakes against
those under-reporting food intake, we find all food categories under-reported.

This issue of energy
under-reporting is dismissed by nutritional epidemiology on the grounds that
all their propsed statistical associations of diet and disease are adjusted for
all of those factors of importance in under-reporting (body weight, energy
intake, gender, age etc). However, there is an increasing number of researchers
who are showing that this statistical adjustment is flawed when it comes to
under-reporting food intake. Basciaclly, an average daily intake of a food is
composed of three elements. Firstly, the population average embracesboth consumers and non-consumers of the
food in question. Some people who under-report energy intake may simply deny
eating one or more foods. That is the first route of under-reporting. The
second is that they admit reporting but under-report the frequency of
consumption. The third is that they admit eating the food, are truthful about
the frequency of intake but are untruthful with the portion size they report.
Of course any combination of these is possible. There is simply no way in which
statistical jiggery-pokery can unravel this web of deceit. So we have only one
option. We create a cut off point (RMR + 15% of RMR) for energy requirement and
anyone falling below this is excluded from the analysis. Its painful to lose
subjects in this way when statistical power is dependet on adequate numbers.

Without doubt the
area of greatest concern over the distorting impact of energy under-reporting
is in relation to obesity. Firstly, the scale of under-reporting rises
considerably with rising body weight. Secondly, obesity is such a hot topic as
regards candidate foods for taxation or labeling. How can we be so confident in
shaping public health nutrition policy in obesity when (a) we know that food
under-reporting is generally a problem but particularly a problem in obesity
and (b) when there is no hope of any statistical trick separating out the three
lines of mis-reporting: denying ever eating the food in question, not
accurately reporting frequency of the intake of a target food and finally,
under-reporting portion size. It bothers me a lot but its a mere nuisance to
the high priests of public health nutrition who know boththe problem and the solution.

Monday, December 5, 2011

John Minnoch (1941-1983) lived in Seattle and is credited in
the Guinness Book of Records as being the heaviest male in history. At 6 feet 1
inch tall, he weighed 442kg, equivalent to a BMI of 128. That equates to the
biomass of just 4.5 Irish adult males! Now when we talk about the epidemic of
obesity, there is a possibility that some people might think that a significant
fraction of the population would reach the weight of John Minnoch. That is not
how it works. Several years ago Steve O’Rahilly, Professor of Medicine at
Addenbrooke’s Hospital Cambridge and a world authority on the genetics of
obesity, raised the possibility that the epidemic of obesity was beginning to
level off in the UK. Thus, faced with an obesogenic environment, the population
variation in genetic predisposition to obesity is such that those who can cope
with this environment will remain within the normal weight range while those
susceptible to an obesogenic environment will attain a level of over weight or
obesity up to their genetic potential.
Two recent papers now put flesh on O’Rahilly’s speculation.

The first of these papers gathered data on time trends in
obesity over the period 1999 to 2010.The authors of the paper[1],
from the Institute of Preventative Medicine at Copenhagen, set out a total of 7
criteria, which had to be met if a published study was to be included in their
analysis. For example, the sample size had to be greater than 5,000 and data on
weight and height had to be measured directly and not self reported. Thus out
of 52 studies, only 44 met the 7 inclusion criteria. They also graded the
studies into very high, high, medium or low quality. Of the 6 studies graded
very high quality data, 5 showed that obesity rates were stable during the
period 1999 to 2010. These 5 were from France, Sweden, England, Greece and
Australia and only in China did a very high quality study show an in crease in
obesity. Among children and adolescents, there was a clear trend toward a
stabilization of obesity across continents and while the pattern among adults
was less clear-cut, nonetheless, stabilization was generally evident.

The second study comes from Australia, actually from a
rather distinguished WHO Collaborating Centre for Obesity Prevention, and it
looked at obesity trends in preschool children over the period 1999 to 2007[2].
They studied two cohorts, one aged 2 years old in 1999 (130,000) and the other
3.5 years old in 1999 (96,000), each of which was followed annually to the year
2007. Weight, height (and length for younger age groups) were measured
annually. Whereas in 1999, some 2.5 % of 2 year olds were obese, in 2007, this
fell to 1.7%. For three year olds in 1999, the comparable figures were 4.5% and
2.9%. Similar trends were seen when obese children were combined with over
weight children (from 13.5% to 12.4% in the 2 year old cohort and from 18.5% to
15.4% in the 3.5 year old group over the period 1999-2007). Although the
overall rate of obesity and overweight was higher in the lower socioeconomic
groups, the rate of decline in fatness was highest in these groups.

The first study would suggest that, as expected, the
variation in the genetic potential to develop obesity would ultimately be met
and that the prevalence rate would stabilize. It doesn’t mean the problem has
gone away since obesity will continue to be a major drain on the economics of
our health care systems. What it will do is to increase the focus on the
management of the physiological disadvantages of obesity and overweight and in
that regard, a greater emphasis on the promotion of physical must emerge, since
nothing compares with physical activity as an antidote to the adverse effects
of obesity. In the case of the Australian study of preschool children, the data
suggests that there is a greater awareness of the problem of obesity among
parents, particularly those who are socially disadvantaged. Preschool children
do not make their own food choices so this reflects a mind change of mums and
dads. Whether this all translates into fewer obese adolescents remains to be
seen.

Monday, November 28, 2011

Sir Peter Medawar,
Nobel Laureate in immunology and philosopher of science once wrote: “If
politics is the art of the possible, then science is the art of the soluble”.
The great trick in science is to manipulate the experimental conditions in such
a way that the potential solution becomes accessible. Today, I will document
two examples of discovery in nutritional science showing indeed the ingenuity
of the mode of discovery but also the happenstance of scientific discovery. Lets
begin with the ingenuity.

Atmospheric carbon
dioxide is comprised predominantly by the stable form of carbon, designated 12C.
Radioactive carbon is a heavier for designated 14C. Above ground nuclear
testing began in 1955 and continued until a limited nuclear test ban treaty
came into effect in 1963. During this period, atmospheric CO2 became
more enriched with 14C than normal and when the ban was enacted,
those levels plummeted, not because of the decay of the radioactivity (14
carbon has a half life of 5,700 years) but because this CO2 was
absorbed into the earths biomass. Ultimately, everything we eat comes from this
biomass so we were exposed and thus enriched ourselves in the radioactive form
of carbon (14C) but at miniscule levels of no biological hazard. Even though
the amounts in us are trace, smart physicists can measure the ratio of 14C to
12C. If a cell is created during the period when 14C is high then we can track
the life cycle of such cells by seeing how soon the ratio of the radioactive form
to the normal form returns to pre-nuclear testing levels. A fast return means
that the cell has a short half-life. A slow return means that the cell has a
long half-life. By recruiting people born before, during and after the above
ground nuclear tests and following them over time, a group of scientists at the
Karolinska Institute (Nature October 6th 2011) were able to show
that fat cells have a life of about 10 years and the fat within that cell is
renewed 6 times during this period. That means that the fat within the cell has
a life of about 1.6 years. The same group using this technique also showed that
in fat people, the life of a fat cell is shorter and also that when people
diet, the number of fat cells remains constant. The data are extremely useful I
understanding the dynamics of fat metabolism over decades and surely, this
bunch of smart Swedes must get recognition for their “art of the soluble”.

Let us now turn to happenstance in
scientific discovery. Justus von Liebig
(1803 - 1873) is generally regarded as the father of food chemistry. Like many
of the leading academics of today, he was an entrepreneur. Together with a
Belgian scientist, George Giebert, he developed a means of concentrating beef
into a nourishing beef extract. Because European beef was expensive, he located
his manufacturing plant in South America.The Liebig Extract of Meat Company traded as Lemco and after his death,
the product evolved into Oxo, a beef extract now owned by Unilever. Liebig also
turned his technological know how to brewer’s yeast, managing again to
manufacture a nutritious concentrate. Ultimately, a British company, The
Marmite Food Extract Company, would manufacture this extract and sell it as the
Marmite we know today. Incidentally, Unilever also now own the Marmite brand.
Marmite has a special place in the history of nutrition with very significant
links to major public health issues of today.

That story starts in the slums of Bombay, as it
was known then, and a rampant form of anaemia, common among female workers in
the textile factories. A young British medical doctor specialising in clinical
chemistry, Lucy Wills, was persuaded to take up this challenge. She began by
ruling out infection and infestation and ascertained that the form of anaemia
was macrocytic anaemia, an inadequate number of red blood cells. She then
turned her attention to the diet of these poor women and using monkeys as
experimental models was able to induce this form of anaemia in the monkeys by
feeding the bland and rice dominated diets eaten by the women. Vitamin A and
Vitamin C had just been discovered and she quickly ruled them out as causative
factors.

Now ex-pats love a bit of home comfort and
Marmite was as British as these comforts come. One can imagine Dr Wills sitting
in her lab among cages of monkeys, one of whom would somehow charm her to
become her little pet. And it’s not impossible to imagine that she would let
this particular monkey share a bit of Marmite at lunchtime. But it is difficult
to imagine her utter shock and surprise when alone among the anemic monkeys,
this one recovered.However, from
this unplanned experiment of n = 1, she simply moved directly to her patients
and gave them Marmite. Their anaemia was cured. It was 1941 before Roger
Williams of the University of Texas identified folic acid as the active vitamin
in green leafy vegetables that cured macrocytic anaemia (folium is the Latin for leaf). Two years later, at Lederle
Pharmaceutical (now part of Pfizer) from one and a half tons of liver, folic
acid crystals were isolated and the first synthetic folate was made.

Ethical approval for mass exposure to miniscule
levels of ionising radiation is unthinkable but the super nuclear powers don’t
need ethical approval to detonate atomic bombs above ground. And, ethical
approval for a clinical trial based on an unplanned experiment with one monkey
is also unthinkable. Science moves in odd ways.

Monday, November 21, 2011

That a society
trusts its scientific community to be truthful in all its manifestations is a
given in any civilised society. We are all aware of scandals involving
sometimes young and sometimes prominent scientists being disgraced for having
falsified scientific data in peer-reviewed scientific publications in scholarly
journals. That is the newsworthy end of this thorny issue but beneath that
headline-catching level lie some equally challenging issues of scientific
integrity. The first of these relates to the belief of many MEPs that
scientific advisers to the European Food Safety Agency (EFSA) should be, as
George Smiley, would have said “Persil grade”, clean as the driven snow with no
links to the food industry.That
pressure has led to several high level confrontations between EFSA and the
European Parliament plus a plethora of NGOs in the food area. Now an expert in
the biology of the lactating yak is unlikely to be considered as a likely
expert for a panel of EFSA but someone with a life’s investment in public
health nutrition research is likely to be very attractive. The problem is that
the lactating yak expert attracts zero interest from the food industry while
the lifetime devotee to public health nutrition cannot be free from food
industry links. If their research is world class, everyone will want to talk
with them, pay their travel to give talks, co- fund or fund their research and
generally get to know such an expert. And if the EU, through its competitive
research programme funds this expert, then for sure, there must be industry
links because that is an absolute requirement of funding. So the MEPs cannot
have it both ways. If they want the best, they will have to accept that both
the regulator and the regulated will visit the best.

Having a link
with the food industry appears to suggest to MEPs that there is a higher
likelihood that independent scientific thinking is likely to be compromised.
However, this does not appear to apply to NGOs. A scientist who is an active
member of an environmental NGO could be compromised if he or she were to be a
member of an advisory committee of an EU institution if the topic involved GM
foods. And would a strict vegan be a truly independent chair of an expert group
on some nutrient, which has a strong line with animal based foods like iron or
zinc? The simple solution here is to require that such potential conflicts of
interest be declared so that anyone reading a report involving such individuals
knows the background of the experts. But that doesn’t count for much with MEPs.
NGOs are inherently good whether they be environmental NGOs or vegan NGOs. It
is only industry that seems to matter to the guardians of scientific integrity.
Seems strange to me!

Finally, we
burrow down to what is ultimately the most sinister aspect of scientific
integrity, namely being honest in interpreting primary (my discovery) or
secondary (your discovery) data. In a very important paper published in the
International Journal of Obesity {2009-(1-50}, researchers at the University Of
Alabama reported a study in which they tracked the manner in which primary data
(my discovery for example) is cited in secondary data (your reported discovery
citing my original findings in support). They chose a study, which examined the
link between the development of obesity and sugar-sweetened beverages (SSBs).
The original primary data showed no statistically significant association
between SSB intake and obesity. Often, authors of papers, which report
“negative” data, grasp at straws of positivity. In this case, a subset analysis
showed a suggestion of such a link. However, the subset analysis was always a
sideshow while the main event, the true objective of the study, showed zilch
evidence linking SSBs and obesity. They then tracked all the studies published
in English that cited the paper. Of these, 84% inaccurately reported the
primary data. That is, they chose to ignore the main and “true” conclusion of
the paper and chose instead to focus on the sideshow, the non-intended analysis,
which did suggest that in some sub-groups there was a possible link between SSBs
and obesity. This is a minor snapshot of a paper that shows a massive
systematic bias of researchers toward that interpretation of data, which suits
their agenda.

Just about
everybody reading this will recognise this bias in all spheres of human
activity. However, for science, which purports to be built on the truth, this
is a major problem. If scientists, select from here and there to suit their
agenda, the “sayonara” objectivity.

Monday, November 14, 2011

Some years ago,
I was given the honour of delivering the opening plenary lecture to the First
World Congress of Public Health Nutrition and I had carte blanche as to the
content. I chose to talk about nutrition and genetics and when I finished, I
was set upon by the doyens of the subject to whom the idea that genes could
play a role in such chronic diseases as obesity was verging on sacrilege. The
argument was simple but fundamentally flawed. Obesity rates, they argued, have
rocketed over the last 50 years[1]
during which time the gene pool has remained constant so how could genes be
involved.Recently, I gave a
similar talk to the Polish EU Presidency gig and got the same reaction. So here
is how it happens. Imagine you could take 1000 extremely muscular Maasai
tribesmen from the utterly non-obesogenic Kenyan plains and re-house them with
a decent disposable income in any western city awash with obesogenic
facilities. Some would resist weight gain. Some would show modest weight gain of
which some would do so quickly and others more slowly. Some would become
overweight and obese and do so at different rates. When the experiment is
finished, I would predict a pattern of body weight among the Maasai broadly
similar to the prevailing local pattern.

The evidence
dates back 30 odd years when three seminal papers were published in leading
medical journals. The first used identical and non-identical children and from
this mix it is possible to say what part of obesity is inherited and what part
is due to the environment. The non-identical twins share the same environment
but not the same genome. In the case of identical twins, they share the same
environment and the same genome.
Geneticists have used this model in many areas to separate out the effects of
the environment and the genome. The outcome was that 70%+ of the variation in
obesity was inherited. The next set of data took identical twins that were
overfed for several months and later, underfed for several months. In the
overfeeding phase of 1000 extra calories per day over normal, all subjects
gained weight but to varying degrees. The big variation was between groups of
identical twins. However, among identical twins, here was no variation. If one
gained weight rapidly, so did the other. If one resisted weight gain, so did
the other. And when 1000 calories a day were deducted from their habitual
intake, the same happened. All lost weight but some more than others. And
identical twins shed weight at exactly the same rate. The final study looked at
adoptees and compared their body weights with those of their adopting parents
and those of their biological parents. The correlation was much stronger with
their biological parents.

All of this data
was then buried and forgotten because it was a most inconvenient truth. Even
accepting its truth, those charged with the public health nutrition challenge
of obesity had a further problem. If the average punter got word that their
weight problem was genetic, they would abandon all personal efforts at weight
management, throw their hands in the air and declare “Its not my fault, its my
genes” as they wolfed into some stylish nosh. One has to have considerable
sympathy for this point of view since the struggle to help manage obesity is a
truly hard road. For a while, there was an escape clause in that it was argued
that “that was then and this is now and thirty + years ago we didn’t have the
ubiquitous obesogenic environment of today”.And that was fine until Professor Jane Wardle of University
College London began publishing data on modern twin cohorts followed up over a
long period and with quite detailed lifestyle and diet recorded. Everything
shown 30+ years ago was shown to be still true today. Moreover, Professor
Wardle also showed that the belief that obesity in children has a huge
socio-economic dimension is just not true. Twins of lean parents remained thin
from aged 4 to 11 years irrespective of social class. However, when children
from overweight children were considered, those of low social background did
show accelerated weight gain. Thus social class matters in childhood obesity
but only if filtered by the genes they inherited.

Studying twins
helps us to quantify the true rate of heritability of obesity. It doesn’t tell
us which genes are involved and thus it doesn’t allow us to predict which one
of us will put on weight faster and more easily than others. Now, new
technology allows us look at many hundreds of thousands of points of variation
along the human genome to see where this natural variance is most pronounced in
the obese as opposed to those of us lucky to remain lean. Each point of
variation along a gene is known as an allele and there are certain alleles,
which are much more commonly found among the obese. Thus we are now approaching
the point where we can predict that a certain individual has a strong genetic
tendency toward obesity and maybe, that knowledge could be used to help
children and parents to take preventative measures against obesity. The
converse is also true. We can now conduct simple genetic tests that will
indicate the best calorie reduced diet for individuals to follow in losing
weight. Some will do best by shedding fat calories and other will do best
shedding carbohydrate calories. For some, either route will be equally
effective.

When one
mentions the link between genes and obesity, attention always turns to genetic
variation influencing how energy rich substrates are handled (digested,
transported stored, retrieved, metabolized and so on) in the body. However, this
is simply because the people with the biggest interest in genetic research are
usually biologists. But a genetic tendency to become obese may relate to our
behaviour, our food choice, our satiety, our will power and any one of the many
aspects of our lives that govern food intake. That poses an even greater
challenge to the study of diet and obesity.

As to the
extension of nutrition and genetics to the wider area of personalised
nutrition, take a look at the website of an EU funded project that I am coordinator:
www.food4me.org.

[1] Actually the rocketing
started in the 1850s but that’s another story

Sunday, November 6, 2011

There is at
present a considerable media interest in the taxation of both fat and sugar in
an attempt to control the epidemic of obesity. In a typical Western diet, fat
and sugar combine to contribute about 55% to 65% of our total caloric intake.
To contemplate putting a tax on more than half our energy intake is palpably
absurd so the target is then moved toward specific foods which merit taxation
based on (a) their fat and sugar levels and or (b) their putative contribution
to obesity. The problem regarding the latter is a total lack of any evidence
linking very specific food groups to obesity.Across time(decades of research) and space (all continents) there is no universal
single pattern of food choice uniquely associated with obesity. Consider a
solid example of how this works. Across time and space, every study that has
sought to examine the link between dental caries and diet has found that it is
the frequency of sugar consumption, which is important.When, time after time, in all
corners of the globe and under all sorts of different circumstances an
observation is found to be simply constant, then it ends up in the “no-brainer”
category of knowledge. Not so with obesity. There is no consistent pattern of
food intake. Some eat excessively and never eat chips, others eat chips but
don’t eat excessively and you can substitute “chips” in that phrase with any
food you like. If there were a pattern that every researcher saw every time
they looked we’d have done something about it long ago. However, there simply
is no consistent pattern of food choice that is uniquely linked to obesity.

Of course that
is a great disappointment to those who hold the belief that obesity is directly
related to the intake of fast food or to foods with empty calories, high in
sugar or fat. Having an identifiable corporate whipping boy makes life easy.
Bashing McDonalds might make some concerned citizens feel good but since
McDonalds are responsible for the sale of maybe just 10% of all chips consumed,
ignoring the main purveyors of chips (ethnic restaurants, fish and chip shops,
pubs, works canteens, mobile food vendors etc) means that the real “villains”
are getting away “Scot free”. And of course when it comes to the practicality
of imposing a fat tax on chips (and other fast foods), the taxing of bars, fish
and chip shops and the other suppliers of the nation’s chips poses quite a
logistical problem.

In the absence
of hard data to identify foods, which are uniquely involved in the development
of obesity, the next step is to use the nutritional composition of foods to
sort out those that are high in those nutrients for which we should reduce our
intake. This is referred to as “nutritional profiling”.The theory here is that a mathematical
formula can be devised into which the nutritional properties of individual
foods are entered allowing an output which marks foods into “good”, “bad” and
“ok but not great” categories. In the UK the dream is to then assign a colour
code to this as per traffic lights. Interestingly, when the mathematical
construct gets things wrong, that is to say when it disagrees with the a priori opinion of the users, the
formula is changed to make sure that the output meets the opinions of the
particular experts who are adherents to this process. In principle, anything
that helps consumers to make better choices must be welcome but the problem
here in the EU is that the process is doomed to poor science for the simple
reason that we do not use portion sizes here but rather units of 100g or 100
ml. The argument is that across the EU, portion sizes differ. For example, it
is argued that in Italy, the average intake of pasta is 3 to 4 times higher
than in Northern EU. However, this difference is not due to portion size but to
the frequency of consumption. A plate of pasta in Rome is the same as a similar
plate in any Italian restaurant across the entire EU. Mixing up frequency of
consumption (higher for pasta in Italy) with portion size is nonsense but that
is at the heart of the EU thinking as regards EU food legislation. In the US
there is an agreed RACC (Recognised Amount Commonly Consumed) value for each
food. To understand how daft this is, consider the comparison of water biscuits
(usually served with cheese) and pizza. A typical 100-gram of pizza will
provide about 7 grams of fat while 100 grams of water biscuits provide up to 23
grams of fat. However, a typical serving size of pizza would yield about 20+
grams of fat while a typical serving of water biscuits would contain about 4 grams
of fat. Ignoring portion size can penalise foods, which have typically small
servings Per 100g, mustard has twice as much fat as full fat milk!!!!!

Trying to find a single all embracing
formula to assign a general nutritional quality index to every food is
difficult and will be constantly bothered by obviously “wrong” decisions. An
approach used successfully in Scandinavia, uses an agreed compositional target
per food category. If there is a move toward a reduction of a given nutrient,
then the regulators and the manufacturers of a particular category of food can
agree a target that all can work towards. In Scandinavia, foods that reach that
target get to display an emblem which consumers can recognise as having met a
given standard.

One of the first
lessons to be learned in nutrition is that there are no such things as “good
foods” or “bad foods” but rather “good diets” and “bad diets”. Sadly, it is a
lesson quickly forgotten by those who regard diet and obesity as a simple
problem linking certain naughty foods with weight gain.

Tuesday, November 1, 2011

The media is today awash with articles on all aspects of food and health and some are so non-sensical that I thought I'd start my own blog to provide an alternative medium through which an informed view on food and health can be delivered. The blog will be a weekly event coming live every Monday morning, beginning on Monday November the 8th and will cover a wide range of topics.

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"Ever seen a fat fox ~ Human obesity explored"

About Me

I graduated from University College Dublin in 1971 with an Masters in Agricultural Chemistry, took a PhD at Sydney University in 1976 and joined the University of Southampton Medical School as a lecturer in human nutrition in 1977. In 1984 I returned to Ireland to take up a post at the Department of Clinical Medicine Trinity College Dublin and was appointed as professor of human nutrition. In 2006 I left Trinity and moved to University College Dublin as Director of the UCD Institute of Food and Health. I am a former President of the Nutrition Society and I've served on several EU and UN committees on nutrition and Health. I have published over 350+ peer reviewed scientific papers in Public Health Nutrition and Molecular Nutrition and am principal investigator on several national and EU projects (www.ucd.ie/jingo; www.food4me.org). My popular books are "Something to chew on ~ challenging controversies in human nutrition" and "Ever seen a fat fox: human obesity explored"